The neuronal cell-specific alternative splicing regulated by SFPQ/NeuN was impaired in the ALS patient samples, demonstrated by the increased isoforms of the NMHCII-B transcript excluding the N30 exon and the concurrent decreased level of the NMHC II-B protein in the ALS patient cerebellar cortex tissues. Here, SFPQ is linked to amyotrophic lateral sclerosis.